ArticleJournal of advanced research2026
Histone H4 lysine 12 lactylation-driven ZIP14 expression is involved in electroacupuncture therapy against cerebral ischemia/reperfusion injury in mice.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Iron, Copper, and Zinc Dyshomeostasis in Cardiovascular and Cerebrovascular Diseases: Redox Mechanisms, Evidence Levels, and Translational Prospects.International journal of molecular sciences · 2026Review
- Histone lactylation-mediated glycolysis-ferroptosis axis in neurological diseases.Frontiers in molecular neuroscience · 2026Review
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionElectroacupuncture (EA) has been demonstrated as an effective therapeutic intervention for cerebral ischemia-reperfusion injury (CIRI); however, the fundamental processes underlying EA therapy remain largely elusive, which hinders the optimization and broader clinical application of EA. It has been reported that during CIRI, cellular metabolism undergoes a shift from oxidative phosphorylation to glycolysis, giving rise to an accumulation of lactate, but whether and how lactate is involved in CIRI and EA therapy is not fully understood.
objectivesTo explore the role of lactate in EA therapy against CIRI and the underlying mechanisms.
methodsNeurological outcome evaluations and TTC staining were performed to assess CIRI in mice. Western blotting and immunofluorescence were used to detect histone lactylation, and genes regulated by histone lactylation were identified by CUT&Tag, ATAC-seq and RNA-seq, followed by investigation of the role(s) of an iron transporter encoding gene Zip14 in EA therapy. Arterial lactate levels in stroke patients were assessed 30 min after recanalization using arterial blood gas analysis.
resultsLactate markedly enhances histone H4 lysine 12 lactylation (H4K12la) in neurons, concomitantly upregulating PKM2 expression-a pivotal regulator of lactate production. EA protects neurons in the ischemic penumbra and improves neurological outcomes following CIRI by suppressing PKM2-mediated H4K12la. Furthermore, CIRI elevates H4K12la enrichment at Zip14, which facilitates chromatin accessibility, activates Zip14 transcription, and ultimately triggers ferroptosis. EA treatment attenuates ferroptosis and mitigates CIRI by decreasing ZIP14 expression. Clinically, EA significantly reduces arterial lactate levels after recanalization in patients with ischemic stroke.
conclusionsThis study uncovered a previously unrecognized mechanism by which lactate is involved in EA therapy against CIRI, highlighting H4K12la-dependent ZIP14 expression as a potential therapeutic target for CIRI management and EA optimization.
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